Analysis of molecular structure of inward rectifier K channel consisting of three subchannel

在对使用贴片钳方法使用乳腺大鼠肠道myocytes进行的分析中，以保持心脏细胞转移到超极化化的膜潜力。超极化化在中等脂肪期被剥夺的自动观测到中脂肪期，并保持膜潜力稳定。在全细胞电压钳中，输入记录器KI-D1 + I-D1当前（IK 1）在发展期内被研究生增加，然后在中间阶段与12个文件夹比较。因此，超极化可能是由IK 1中的增量产生的。在IK 1中增加的机制在执行单通道记录时并不容易。在开发周期内，它将不会被观察到，因为一种类型的渠道显示出在数量的通道或开放概率上的增加。在较后的胎儿期，通道通常比在中间的胎儿期打开更大的单元的行为。在基因编码IK 1通道（Kir 2家族）的分析中，Kir2.1和Kir2.2在大鼠心肌细胞中表达。定量PCR方法显示了Kir2.2表达在17-文件中增加的Kir2.1从中间到更后一个脂肪周期中只发现2-文件。因此，这些数据建议Kir2.2信道编码的IK 1信道是预测在fetal开发期间，然后产生ventricular cardiomyocytes的超极化。

In an analysis of fetal rat ventricular myocytes using the patch clamp method, resting membrane potential of the cardiomyocytes shifted to hyperpolarization. The hyperpolarization during the fetal period abolished automaticity observed in middle fetal period, and kept resting membrane potential stable. In whole-cell voltage clamp, the inward rectifier KィイD1+ィエD1 current (IK1) gradually increased during the developmental period, and then was 12-folds comparing that in the middle fetal period. Therefore,the hyperpolarization may be produced by the increase in IK1. Mechanisms of the increase in IK1 was understood not to be simple when single channel recording was performed. During the developmental period, it was not observed that one type of channel showed an increase in the number of channels or in open probability. In the late fetal period, channels possessing larger unit conductance than that in the middle fetal period opened frequently. In analysis of gene coding IK1 channels(Kir 2 family), Kir 2.1 and Kir 2.2 were expressed in rat fetal cardiomyocytes. The quantitative PCR method showed that expression of Kir2.2 increased in 17-folds in spite of only 2-folds increase in Kir 2.1 from the middle to the later fetal period. Therefore, these data suggest that IK1 channel coded by Kir2.2 becomes predominant during fetal development, and then produces hyperpolarization of ventricular cardiomyocytes.